Sunday, March 11, 2012

A young man presented after a prolonged seizure. He had had a fight with his girlfriend, and she thinks he ingested something, thinks it was ecstasy (MDMA) but might have been other things.

The patient was unconscious. He was intubated. He had a combined respiratory and metabolic acidosis, with pH 6.98, pCO2 of 65 and HCO3 of 15. K was normal. Blood pressure was 180/80. There was no pulmonary edema or hypoxia. Cardiac Echo showed excellent hyperdynamic function. Here was his initial ECG:

You have little to lose by shocking (safe even if sinus, but best not to shock sinus tach)

Must be able to safely do procedural sedation

If converts, then recurrence after cardioversion requires antidysrhythmic medication

This patient had an ingestion and seizure, is young and has a hyperdynamic heart with good function. He could have VT due to his ingestion, but sinus tach is far more likely.

Here is the same ECG with some annotation (lines):

The first line is drawn at the onset of the QRS in V2, which is clear. I draw this down to the bottom lead II rhythm lead to show where the onset of the QRS is in lead II. Then you can draw analogous lines for all other leads. The QRS duration appears to be closer to 120 ms, arguing strongly against VT. There is a superior axis (about -90 degrees). The duration from the onset of the R-wave to the nadir of the S-wave in V2 and V3 is about 60 ms, which argues strongly against VT. There is a tall R-wave in aVR, consistent with sodium channel blocking effects of toxins. This is unlikely to be VT.

The clinicians shocked the patient at 200 J x 2, with no change. They administered sodium bicarb as antidote for Na channel blocking effect. Then, with supportive care and fluids, over the next 10 minutes, the heart rate slowly and gradually decreased to 150. Here is the subsequent ECG:

This is clearly sinus tach. The QRS duration has shortened a bit, but there is still a large R-wave in aVR. The axis is still superior. The morphology of the QRS has not changed, confirming that the previous rhythm was supraventricular.

In this case, the first ECG has no obvious p-waves, but they may be there and difficult to discern. As the patient is not hemodynamically unstable, it is reasonable to give some supportive care and wait to see what happens. When the rate gradually falls, as in this case, then it must be an automatic, not re-entrant, rhythm. Re-entrant rhythms are constant, though can be affected by antidysrhythmics.

That the morphology of sinus is the same as in the initial ECG makes an SVT, including sinus, definite.

That it fell gradually strongly supports sinus as the initial rhythm.

Outcome: the patient recovered uneventfully. The drug screen, including chromatography for 4000 different substances, was negative for all except pseudoephedrine. However, many toxins do not show up on tox screens.

First 3 are complex and I find difficult to apply. All (except Sasaki's, for which as far as I know there has been no validation attempt) have fared substantially worse in validation than in derivation.

I put in a little effort to make the diagnosis based on these algorithms, but don’t obsess on it.

Management

If you're not sure, but pretty sure it is not sinus tach

Sedate/Cardiovert (or Adenosine)

Adenosine if you suspect SVT:

---Older, with known absence of structural heart disease

---Young age, unless known heart disease

---QRS < 140 ms

---No obvious signs of VT

concordance, fusion beats, AV dissociation

---Unequivocal rapid depolarization of the initial part of the QRS (e.g.,
normal LBBB or RBBB)

For those who don't understand this comment: By Vi>Ve, this comment refers to the following:

--it is an index of slow conduction at the beginning and at the end of the QRScomplex by estimation of initial (vi) and terminal (vt) ventricularv activation velocity ratio (vi/vt), obtained by measuring the voltage in millivolts on the ECG tracing the impulse travelled vertically during the initial 40 ms (vi) and the terminal 40 ms (vt) of the same bi- or multiphasic QRS complex.

Sometimes I find this relatively easy to determine, but not in this case. And so the newer Vereckei rule using aVR only is easier, and Sasaki's rule easier still.

By Sasaki:

1) Initial R in aVR? --No, go to 2)2) In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)? No, go to 3)3) Initial r or q ≥ 40 ms in any lead? --No, therefore it is SVT.

So you are probably right, but I don't see it and think that in this case that rule is hard to apply.

Troy, thanks for the comment. LAFB should have a tall late R-wave in lead I, but in this case the late deflection is negative in lead I and positive in lead aVR. This is right ventricular conduction delay which is common in intoxication with sodium channel blockers, which tend to affect the right bundle more than the left. This often leads to a late high voltage R-wave in aVR, and sometimes also an R' wave in V1 (not seen here), sometimes with a Brugada-like pattern.

do you find fluid to be useful enough in many less emergent situations to be a tool to help make the determination of the rhythm? it seems to me that many non-reentry tachyarrhythmias slow down a bit with fluid administration, but i don't see it being regularly used by clinicians.

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